Our working hypothesis is that lymphokines and in particular interleukin-2 (IL-2) may affect pituitary hormone release. The pituitary hormone, adrenocorticotropin (ACTH) was our first candidate to be modulated by IL-2. The adrenal steroids inhibit lymphocyte function so we reasoned that IL-2 might feedback positively releasing ACTH and dampening lymphocyte activity. This may be a homestatic feedback loop between the pituitary and the immune system. The simplest system to test this hypothesis was in vitro. Preliminary results indicate that mouse IL-2 caused a significant release of ACTH in vitro. Further investigations are required to determine if the ACTH released by IL2 is specific and to test IL-2 action on other neuroendocrine tissue.